HICNet Medical News Digest Sat, 24 Sep 1994 Volume 07 : Issue 46 Today's Topics: [MMWR 16 Sept 94] Inadequately Filtered Drinking Water [MMWR] Salmonella enteritidis associated with Home Made Ice Cream Reflections on First International Symposium on Brain Death +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-1165 Internet: mednews@stat.com Bitnet: ATW1H@ASUACAD Mosaic WWW: http://biomed.nus.sg/MEDNEWS/welcome.html Compilation Copyright 1994 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. Associate Editors: E. Loren Buhle, Jr. Ph.D. Dept. of Radiation Oncology, Univ of Pennsylvania Tom Whalen, M.D., Robert Wood Johnson Medical School at Camden Douglas B. Hanson, Ph.D., Forsyth Dental Center, Boston, MA Lawrence Lee Miller, B.S. Biological Sciences, UCI Dr K C Lun, National University Hospital, Singapore W. Scott Erdley, MS, RN, SUNY@UB School of Nursing Jack E. Cross, B.S Health Care Admin, 882 Medical Trng Grp, USAF Albert Shar, Ph.D. CIO, Associate Prof, Univ of Penn School of Medicine Martin I. Herman, M.D., LeBonheur Children's Medical Center, Memphis TN Stephen Cristol, M.D., Dept of Ophthalmology, Emory Univ, Atlanta, GA Subscription Requests = mednews@stat.com anonymous ftp = vm1.nodak.edu; directory HICNEWS FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- Date: Sat, 24 Sep 94 16:07:45 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR 16 Sept 94] Inadequately Filtered Drinking Water Message-ID: Assessment of Inadequately Filtered Public Drinking Water -- Washington, D.C., December 1993 The risk for waterborne infectious diseases increases when filtration and other standard water-treatment measures fail. On December 6, 1993, water-treatment plant operators in the District of Columbia (DC) began to have difficulty maintaining optimal filter effectiveness. On December 7, filter performance worsened, and levels of turbidity (i.e., small suspended particles) exceeded those permitted by U.S. Environmental Protection Agency (EPA) standards. On December 8, DC residents were advised to boil water intended for drinking because of high municipal water turbidity that may have included microbial contaminants. Although adequate chlorination of the DC municipal water was maintained throughout the period of increased turbidity, the parasite Cryptosporidium parvum is highly resistant to chlorination. Because of the increased risk for infection with this organism and other enteric pathogens, the DC Commission of Public Health and CDC conducted four investigations to determine whether excess cases of diarrheal illness occurred because residents drank inadequately filtered water. This report describes the results of these investigations. The investigations included a random-digit-dialed telephone survey of DC residents and retrospective reviews of records from two emergency departments, two nursing homes, and seven hospital microbiology laboratories. The occurrence of diarrheal illness or presence of organisms in stool during the 2 weeks before the turbidity violation (period 1: November 22-December 5) was compared with that during the 2-3 weeks after the violation was first noted (period 2: December 6-December 21 or 26). The incubation period for cryptosporidiosis typically ranges from 2 to 14 days. Telephone survey. The telephone survey sampled 1197 household members (0.2% of DC's 600,000 residents) from 462 households in all 22 DC residential ZIP code areas. The percentage of persons who reported having diarrhea (i.e., three or more loose or watery stools in a 24-hour period) were similar for period 1 (the reference period) and period 2 (2.8% versus 3.5%, respectively; relative risk [RR]=1.2; 95% confidence interval [CI]=0.8-1.9). A total of 37% of persons reported that bottled water was their principal source of drinking water at home, and 30% reported that bottled water was their primary source of drinking water both at home and at work. For both periods, reported use of bottled water was similar for persons with and without diarrhea. Hospital emergency department survey. During the two periods, totals of 2140 (period 1) and 3315 (period 2) persons were evaluated at two DC hospital emergency departments. Medical records were reviewed for all persons with diagnoses suggestive of gastrointestinal illness* (104 and 211 persons for periods 1 and 2, respectively). The percentage of all persons who had diarrhea recorded in their emergency department charts was similar for periods 1 and 2 (1.5% versus 2.0%; RR=1.3; 95% CI=0.9-2.0). For both periods, approximately 70% of patients with diarrheal illness were DC residents. The percentages of stool specimens that were positive for enteric pathogens (i.e., bacteria, parasites, or rotavirus antigen) were similar for the two periods. During each period, two stool specimens were examined for Cryptosporidium: none were positive during period 1, and one was positive during period 2. Nursing home survey. Medical records were reviewed for all 443 residents from two selected nursing homes (14% of the 3156 nursing home beds in DC). During both periods, the mean numbers of bowel movements per person per day were 1.3. In addition, the daily mean number of residents with loose or large-volume bowel movements were similar (27.1 and 27.8 persons for periods 1 and 2), and antidiarrheal medications were given at the same rate (0.002 doses per person per day) during both periods. Microbiology laboratory survey. Data were obtained from microbiology laboratories of seven (64%) of the 11 DC hospitals. Although the total number of stool specimens examined for Cryptosporidium increased from period 1 (32 specimens) to period 2 (54 specimens), the percentage positive was lower--but not statistically different--for period 2 (12.5% versus 7.4%; RR=0.6; 95% CI=0.2-2.2). The percentages of stools positive for other pathogens (i.e., bacteria, Giardia lamblia, and rotavirus antigen) were similar for both periods. Reported by: MN Akhter, MD, Commissioner, ME Levy, MD, District Epidemiologist, C Mitchell, R Boddie, District of Columbia Commission of Public Health. N Donegan, B Griffith, M Jones, Washington Hospital Center; TO Stair, MD, Georgetown Univ Medical Center, Washington, DC. Epidemiology Br, Div of Parasitic Diseases, National Center for Infectious Diseases, CDC. Editorial Note: To ensure safe municipal drinking water supplies, water-treatment programs employ multiple barriers to prevent contaminants from reaching the consumer. These barriers include protection of the watershed, chemical disinfection, and filtration of surface water supplies such as lakes and rivers. When one of these barriers is absent or fails, the risk for waterborne disease may increase. The failure of the filtration process in DC prompted particular concerns about contamination with and exposure to Cryptosporidium. Outbreaks of cryptosporidiosis resulting from surface water contamination have occurred when turbidity was 0.9-2.0 nephelometric turbidity units (NTU)**. For example, in a waterborne outbreak in Milwaukee in 1993, a peak turbidity of 1.7 NTU was associated with illness in approximately 400,000 persons (1). In DC, the turbidity levels reached 9.0 NTU. Because Cryptosporidium is highly resistant to chlorination, disinfection of water is not a reliable method for preventing exposure to it. The failure to detect increased rates of illness among residents of DC probably reflects the absence of, or presence of only a small number of, oocysts in the water that supplied the municipal water-treatment plant at the time the filtration failure occurred. In addition, the investigations in DC did not detect any increase in diarrheal illness associated with the elevated water turbidity; however, the sample sizes in these investigations were too small to rule out low-level transmission of waterborne agents. For example, the telephone survey probably would not have detected an outbreak affecting fewer than 12,000 persons. Cryptosporidium is present in 65%-87% of surface water samples tested throughout the United States (2,3). However, because current techniques to detect Cryptosporidium in water are cumbersome, costly, and insensitive, tests to detect it are not routinely performed by water utilities. During 1995, EPA plans to collect additional information about Cryptosporidium and other microorganisms in surface water used by municipal water-treatment facilities in the United States and to assess the effectiveness of water-treatment methods for removing them.*** The early detection of waterborne outbreaks of cryptosporidiosis is difficult for at least four reasons: 1) many physicians are unaware that Cryptosporidium can cause watery diarrhea; 2) the symptom complex often resembles a viral syndrome; 3) clinical laboratories often do not routinely test for Cryptosporidium when a physician requests a stool examination for ova and parasites; and 4) few states include cryptosporidiosis as a reportable disease. Variations in recommendations regarding the duration of boiling during boil-water advisories have reflected uncertainty about how long some organisms can survive. On the basis of a recent literature review, CDC and EPA recommend that water be rendered microbiologically safe for drinking by bringing it to a rolling boil for 1 minute; this will inactivate all major waterborne bacterial pathogens (i.e., Vibrio cholerae, enterotoxigenic Escherichia coli, Salmonella, Shigella sonnei, Campylobacter jejuni, Yersinia enterocolitica, and Legionella pneumophila) and waterborne protozoa (e.g., Cryptosporidium parvum, Giardia lamblia, and Entamoeba histolytica [4-7]). Although information about thermal inactivation is incomplete for waterborne viral pathogens, hepatitis A virus--considered one of the more heat-resistant waterborne viruses (8)--also is rendered noninfectious by boiling for 1 minute (9). If viral pathogens are suspected in drinking water in communities at elevations above 6562 ft (2 km), the boiling time should be extended to 3 minutes. References 1. Mac Kenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med 1994;331:161-7. 2. Rose JB, Gerba CP, Jakubowski W. Survey of potable water supplies for Cryptosporidium and Giardia. Environmental Science and Technology 1991;25:1393-400. 3. LeChevallier MW, Norton WD, Lee RG. Occurrence of Giardia and Cryptosporidium spp. in surface water supplies. Appl Environ Microbiol 1991;57:2610-6. 4. Bandres JC, Mathewson JJ, Dupont HL. Heat susceptibility of bacterial enteropathogens. Arch Intern Med 1988;148:2261-3. 5. Anderson BC. Moist heat inactivation of Cryptosporidium sp. Am J Public Health 1985;75: 1433-4. 6. Bingham AK, Jarroll EL, Meyer EA. Giardia sp.: physical factors of excystation in vitro, and excystation vs eosin exclusion as determinants of viability. Exp Parasitol 1979;47:284-91. 7. Boeck WC. The thermal-death point of the human intestinal protozoan cysts. Am J Hygiene 1921;1:365-87. 8. Larkin EP. Viruses of vertebrates: thermal resistance. In: Rechcigl M Jr, ed. CRC handbook of foodborne diseases of biological origin. Boca Raton, Florida: CRC Press, Inc, 1983:3-24. 9. Krugman S, Giles JP, Hammond J. Hepatitis virus: effect of heat on the infectivity and anti-genicity of the MS-1 and MS-2 strains. J Infect Dis 1970;122:432-6. *Gastroenteritis, diarrhea, nausea, vomiting, gastritis, viral syndrome, dehydration, and hyperemesis gravidarum. **The American Waterworks Association encourages water utilities to maintain turbidity measurements of water as it leaves the treatment plant at or below 0.1 NTU. ***59 FR 6332. ------------------------------ Date: Sat, 24 Sep 94 16:09:00 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR] Salmonella enteritidis associated with Home Made Ice Cream Message-ID: Outbreak of Salmonella enteritidis Associated with Homemade Ice Cream -- Florida, 1993 On September 7, 1993, the Epidemiology Program of the Duval County (Florida) Public Health Unit was notified about an outbreak of acute febrile gastroenteritis among persons who attended a cookout at a psychiatric treatment hospital in Jacksonville, Florida. This report summarizes the outbreak investigation. On September 6, seven children (age range: 7-9 years) and seven adults (age range: 29-51 years) attended the cookout at the hospital. A case of gastroenteritis was defined as onset of diarrhea, nausea or vomiting, abdominal pain, or fever within 72 hours of attending the cookout. Among the 14 attendees, 12 cases (in five of the children and all seven adults) were identified. The median incubation period was 14 hours (range: 7-21 hours); the mean duration of illness was 18 hours (range: 8-40 hours). Predominant symptoms were diarrhea (93%), nausea or vomiting (86%), abdominal pain (86%), and fever (86%). All ill persons were examined by a physician. Salmonella enteritidis (SE) (phage type 13a) was isolated from stool of three of the seven patients from whom specimens were obtained. Eleven of the 12 ill persons had eaten homemade ice cream served at the cookout. No other food item was associated with illness. Testing of a sample of ice cream revealed contamination with SE (phage type 13a). The ice cream was prepared at the hospital on September 6 using a recipe that included six grade A raw eggs. An electric ice cream churn was used to make the ice cream approximately 3 hours before the noon meal. The ice cream had been properly cooled, and no food-handling errors were identified. The person who prepared the ice cream was not ill before preparation; however, she became ill 13 hours after eating the ice cream. Her stool specimen was one of the three stools positive for SE (phage type 13a). The U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service attempted to trace the implicated eggs back to the farm of origin. The hospital purchased eggs from a distributor in Florida. However, the traceback was terminated because the implicated eggs from the distributor had been purchased from two suppliers--one of whom bought and mixed eggs from many different sources. Current USDA Salmonella regulations limit testing of flocks to one clearly implicated flock. Reported by: P Buckner, MPH, D Ferguson, HRS Duval County Public Health Unit, F Anzalone, MD, D Anzalone, DrPH, College of Health, Univ of North Florida, Jacksonville; J Taylor, Office of Lab Svcs, WG Hlady, MD, RS Hopkins, MD, State Epidemiologist, State Health Office, Florida Dept of Health and Rehabilitative Svcs. Foodborne and Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC. Editorial Note: The outbreak described in this report represents the fourth SE outbreak in Florida since 1985; this outbreak is the first in the state to implicate eggs. In the United States, the number of sporadic and outbreak-associated cases of SE infection has increased substantially since 1985; much of the increase can be attributed to consumption of raw or undercooked eggs (1-3). During 1983-1992, the proportion of reported Salmonella isolates that were SE increased from 8% to 19%. During 1985-1993, a total of 504 SE outbreaks were reported to CDC and resulted in 18,195 cases, 1978 hospitalizations, and 62 deaths (Table 1). Of the 233 outbreaks for which epidemiologic evidence was sufficient to implicate a food vehicle, 193 (83%) were associated with eggs. Of these 193 outbreaks, 14 (7%) were associated with consumption of homemade ice cream. No outbreaks have been associated with pasteurized egg products. After eggs are identified by public health officials as the cause of an SE outbreak, USDA attempts to trace the implicated eggs back to the farm of origin to conduct serologic and microbiologic assessments of the farm. If SE is detected on the source farm, the eggs are diverted to pasteurization, or the flocks are destroyed. Under current regulations, USDA can pursue the traceback only if one farm is identified as the source. During 1990-1993, the success rate of USDA tracebacks to the source farm declined from 86% (19/22 outbreaks) in 1990 to 17% (3/21 outbreaks) in 1993. The rate declined primarily because eggs increasingly have been marketed in shipments containing eggs from multiple sources. Although 0.01% of all eggs contain SE and, therefore, pose a risk for infection with SE (4), raw or undercooked eggs are consumed frequently. Based on the Food and Drug Administration (FDA) Food Safety Survey conducted in 1993, 53% of a nationally representative sample of 1620 respondents reported ever eating foods containing raw eggs; of these, 50% had eaten cookie batter, and 36% had eaten ice cream containing raw eggs (S. Fein, FDA, personal communication, September 9, 1994). Many persons may eat raw or undercooked eggs because they are unaware that eggs are a potential source of Salmonella (3) and that certain foods (e.g., homemade ice cream, cookie batter, Caesar salad, and hollandaise sauce) contain raw eggs. Consumers should be informed that eating undercooked eggs may result in Salmonella infection. In addition, eggs should be refrigerated to prevent proliferation of Salmonella if present and should be cooked thoroughly to kill Salmonella. Because most serious ------------------------------------------------------------------------ References 1. St. Louis ME, Morse DL, Potter ME, et al. The emergence of grade A eggs as a major source of Salmonella enteritidis infections: new implications for the control of salmonellosis. JAMA 1988;259:2103-7. 2. Mishu B, Koehler J, Lee LA, et al. Outbreaks of Salmonella enteritidis infections in the United States, 1985-1991. J Infect Dis 1994;169:547-52. 3. Hedberg CW, David MJ, White KE, MacDonald KL, Osterholm MT. Role of egg consumption in sporadic Salmonella enteritidis and Salmonella typhimurium infections in Minnesota. J Infect Dis 1993;167:107-11. 4. Mason J, Ebel E. APHIS Salmonella enteritidis Control Program [Abstract]. In: Snoeyenbos GH, ed. Proceedings of the Symposium on the Diagnosis and Control of Salmonella. Richmond, Virginia: US Animal ealth Association, 1992:78. ------------------------------ Date: Sat, 24 Sep 94 16:13:51 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: Reflections on First International Symposium on Brain Death Message-ID: REFLECTIONS ON THE FIRST INTERNATIONAL SYMPOSIUM ON BRAIN DEATH. (Havana, September 22-25, 1992). By: CALIXTO MACHADO President of the Organizing Committee Correspondence: Dr. CALIXTO MACHADO Instituto de Neurologia y Neurocirugia 29 y D, Vedado, Habana 4 Ciudad de La Habana 10400 Apartado Postal 4268 CUBA Fax: 53-7-336321 E.mail: braind@.ceniai.cu Note: If possible, use E.mail to contact me. The "FIRST INTERNATIONAL SYMPOSIUM ON BRAIN DEATH" was held at the International Conference Center, Havana, between September 22 and 25, 1992. Delegates from twenty-one countries attended this sunny and Caribbean city to discuss many controversial issues concerning brain death and other related states. Argentina provided the biggest delegation (22 attenders). The Opening Ceremony was highlighted by the performance of the National Chorus of Cuba. The singing of beautiful cuban songs prepared the delegates for the words of welcome given by the Organizing Committee, emphasizing that even in such a scientific context, there would be opportunities to discuss human dignity, and life as well as death. On the morning of September 22, delegates enjoyed four striking opening lectures. Like Olympic Gold Medallists, Earl Walker (U. S. A.), Christopher Pallis (U. K.), Gaetano Molinari (U. S. A.) and Daniel Wikler (U. S. A.) followed one another to the rostrum. In his address "Dead or Alive" Earl Walker presented much of the basic material derived from the Collaborative Study of Cerebral Survival sponsored by the National Institute of Neurological and Communicative Diseases and Stroke (1). For ages, people had considered life to exist as long as an individual was breathing. It was later realized that respiration was a means of maintaining the heart which circulated the blood. Life was then attributed to cardio-respiratory action. As long as such activity maintained the nutritional needs of the brain, the individual was alive. But, in the middle of this century, physicians became aware that the brain required much more energy than other organs and, if its needs were not met, it would cease to function, while other parts of the body (requiring less energy) might remain viable and even regain their activity provided the circulation was maintained. The result would be a dead brain in a viable body. Is such a preparation alive or dead? Before answering that question, one had to establish the general principles upon which the diagnosis of a dead brain could be made. The cause of the coma had to be known, so that it could be remedied, if possible. If the condition was not remediable, the state of the brain (underlying all sets of brain-death standards) had to be determined. The clinical status could be ascertained by standard neurological examination. Testing was, however, often complicated by factors such as wounds, which could render it difficult to carry out or difficult to interpret. Other confirmatory examinations then had to be relied upon to establish the death of the brain. But these confirmatory tests had limitations too, some related to the quality of the examination (such as electroencephalo-graphy) and others quantitative aspects (such as isotopic angio-graphy). But with the recognition of these limitations, the available yardsticks provide a satisfactory estimate of the state of the brain. In the rare case in which the clinical and confirmatory test seem to be at variance, observation of the subject for a longer period of time provided clarification of the issue. The validity of these criteria under such circumstances as infancy, concomitant intoxications and impaired cardiovascular status had been questioned. Having established the clinical states of the subject, the physician usually had no problem in certifying death. Problem cases required a careful consideration of medical, religious and legal factors. The second lecture "Brainstem death. Evolution of the Concept", proved a detonator for future discussions. Pallis (2, 3, 4) emphasized that most controversies concerning the criteria for diagnosing death had sprung from a reluctance to define death. Discussions about the validity of different criteria could not meaningfully take place in a philosophical vacuum. What we did (or did not or did not do) in the Intensive Care Unit had to flow from explicitly formulated philosophical premises. "There was only a kind of human death: the irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe (and hence to sustain a spontaneous beat)". All death, in this perspective, was brainstem death. But whereas there was only one death there were clearly several ways of dying. The commonest, by far, was circulatory arrest. But this only proved lethal if it persisted for long enough for the brainstem to sustain irreversible anoxic damage. Circulatory arrest of briefer duration either had no sequelae, or cause slight, moderate or severe neurological damage, the most pronounced form of which was PVS (persistent vegetative state). The death of the brainstem was nearly always the infratentorial repercussion of supratentorial events. It implied the death of the "brain as a whole". A diagnosis of brainstem death had two fundamental implications. The first, pragmatic, was that the heart would inevitably stop, within a relative short period. This was an empirically validated observation, to which no exception had as yet been recorded. The second, philosophical, was that quite independently of the cardiac prognosis an individual with a dead brainstem was already dead (because irreversible unconscious and irreversible apnoeic). The distinctions between "whole brain death" (death of every neuron in the intracranial cavity) and "brainstem death" (death of the "brain as a whole") were, both philosophically and in practice, of minor significance. There were fundamental differences, however, between both of these concepts and the various "higher brain" formulations currently being proposed and discussed mainly by philosophers (5, 6, 7). Their views implied that an individual might be declared dead even if still breathing. We would undoubtedly lose public support for transplantation (and rightly so) if such a proposition were ever seriously put forward. Gaetano Molinari (U. S. A.) was the third on the scene. He emphasized that: "still prohibiting unanimity among physicians worldwide were only some unfortunate but persisting choices of words". Terms like brain death (BD), whole brain death, brainstem death, neocortical death served only to confuse a basic issue, namely, that heartbeat, blood pressure, and even body temperature had lost significance as evidence of life in modern intensive care units. In situations in which spontaneous respirations had stopped but heartbeat persisted, death must be pronounced "neurologically". Comparing the "whole brain" and "brain as a whole" formulations of death, he stated that the only situation in which the British Criteria (8) might declare persons dead while the cerebrum retained functional capacity was the possibility and demonstration in three cases in the American Study (1), and subsequently by others (9), of apnoeic coma with absent cephalic reflexes due to primary brainstem lesions (suggesting death) while electroencephalograms might indicate some residual biological activity (10). The fourth speaker in this marathon was Daniel Wikler, presenting some remarks on "The Philosophical Considerations on Death". Wikler was included as a philosopher, on the professional staff of the President's Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research (11). He asked: "Should we consider a further revision in the definition of death, one which would define death as permanent loss of consciousness? This change would permit physicians to pronounce dead patients in a PVS. Today we lack the ability to diagnose this condition with certainty, so a further change in the law would be unwise. Nevertheless, we might wish to be prepared for the day when physicians acquire the ability to diagnose PVS with certainty, at least for some types of patient. Should such patients be considered dead or alive? A thought experiment suggested the need for a further redefinition. Suppose that, at some future date, doctors became capable of maintaining function in severed heads and decapitated bodies. One poor man, careless in his use of an electric saw, suffers a complete decapitation. His head is carried in an ambulance to the Head Hospital; his body is carried to the Body Hospital in the next town. Since no one can be in two places at once, we must ask: Where is the patient? Is he in the Body Hospital or the Head Hospital? All of us would answer, if we had to make a choice, that he was in the Head Hospital. Now, to continue the story, suppose that the head dies, but that the patient's body continues to live. Is he alive or dead? We cannot say he is alive, since that would imply that at the time his head died he magically switched his location to the Body Hospital. Therefore we must say: he died. At this point in the story, we have his living body, in the Body Hospital, but the patient is not alive. But this is what we have with a patient in PVS; and therefore we ought to say that such a patient is not alive either. In the future, however, we will have to address the problem of those patients who remain in an unconscious state for many years. As an issue in bioethics, the definition of death has been put to rest, but it has not yet expired. In this remarkable lecture Daniel wikler introduced the Symposium to the concept of "higher brain formulations of death" (5, 6, 7). The lunch break was taken up in further discussion: three lunch panels were presented: "Famous Trial Cases" (in relation to BD and persistent vegetative state) was moderated by Gaetano Molinari; "Persistent Vegetative State (PVS)" by R. Firshing (Germany) and "Do not Resuscitate Orders", by Daniel Wikler and Stuart Youngner (U. S. A.). The afternoon of Tuesday, September 22, proved an interesting session in which brain death criteria in different countries were compared. We presented the "Cuban Criteria for Brain Death Diagnosis" (12, 13). These involved a sequential approach for brain death diagnosis, using multi-modality evoked potentials (MEPs) and electroretinography (ERG) as a key step. When reviewing literature it was clear that most sets of criteria had not presented considering such a sequential approach. MEPs and ERG were not usually included as confirmatory tests. The combination of of both a sequential approach, and the application of a test battery comprising MEPs and ERG, could overcome the difficulties posed by conditions traditionally considered as excluding a diagnosis of brain death, and could facilitate clinical practice, in establishing a precise and early diagnosis of BD, which was also fundamental for organ transplantation (14). Christopher Pallis again took the rostrum (he was always expected by the auditorium) and presented the U. K. code (8). The majority of the delegates thought that he had been a member of the Commission that had drawn up the U. K.Code, but we were to learn from him that although the U. K.Code had a brainstem orientation in its concept of death, his own contributions in this field had been due to personal interest and commitment. Pallis stressed that the main emphasis of the U. K. code was the all important question of "context". Unless strict preconditions had been fulfilled, and certain conditions specifically excluded, a diagnosis of brain death could not even considered. He likened the picture to a patient having to pass through two tight sieved, before been tested for brain death. This point had seldom been grasped by those criticizing the code. The scheme outlined was scientifically sound and clinically easy to use. Terminological problems remained however. The memorandum produced by the Conference of Medical Royal Colleges and their Faculties was entitled "The Diagnosis of Brain Death" (8). The document stated, however, that it was the "permanent functional death of the brainstem that constituted death". This is unexceptionable, if taken to mean that death of the brainstem prevented any kind of meaningful functioning of the "brain as a whole". The title of the document remained, however, open to misunderstanding. A different view concerning the U. K. code (8) was presented by a german delegate, Dr. R. Firsching, a close collaborator of R. A. Frowein's. In Germany, death of the entire brain was required and brainstem death alone had not in general been accepted as death of the individual. Firsching emphasized that as recommended by the "Bundersfrztekammer" in Germany, prerequisites for the declaration of brain death were a primary or secondary brain lesion and the exclusion of drug effects, hypothermia or endocrine disorders. After the association of apnoeic coma and cranial nerve arreflexia had been confirmed (in cases of primary supratentorial lesions) four options were available: (1) a waiting period of 12 hours; (2) electrocortical silence as revealed by EEG; (3) step wise abolition of brainstem auditory evoked potentials in sequential investigations; (4) the demonstration of intracerebral circulatory arrest, either by angiography or by transcranial Doppler sonography. In primary infratentorial lesions cortical function might be preserved by hours or days. The demonstration of electrocortical silence by EEG was therefore mandatory. An interesting paper was then presented by a group of colleagues from Argentina. A retrospective analysis of 630 potential donors showed that their average age was 31. There was a net predominance of males (71,4 %). Head injury (46,65 %) and cerebrovascular diseases (44,6 %) were the most common aetiologies among the potential donors. Consent for organ donation was obtained in 58 % of the cases. Preliminary results from a prospective study on BD, were then presented by neurologists from the National Institute of Neurology and Neurosurgery, in Mexico. A warm evening proved a pleasant background to the "Welcome Party". There was plenty of cuban music, rum and friendship. The morning of September 23, began with interesting presentations on: "Neurophysiological Tests and other Confirmatory Techniques in Brain Death and Related States" and "Legal Considerations on Brain Death and Related States". I presented a paper on the "Early Diagnosis of Brain Death Using Multi-modality Evoked Potentials (MEPs) and Electroretinography (ERG)" (14, 15, 16, 17). MEPs and ERG were highly resistant to factors such as: drug intoxication, barbiturate narcosis, the use of anaesthetics, hypothermia, and so on. They had been shown to be reliable in the Intensive Care Unit environment. Considered as single tests, they had their limitations and they had been not routinely included as confirmatory tests for the diagnosis of BD. We applied a battery of tests (including MEPs and ERG) to thirty brain-dead patients. For brain stem auditory evoked potentials (BAEPs), three patterns of abnormality were observed: (1) no identifiable waves (73.34 %); (2) an isolated bilateral wave I (16.66 %) and (3) an isolated unilateral wave I (10 %). For short latency somatosensory evoked potentials (SSEPs) a characteristic pattern was found: absence of N20 and later responses in the scalp-cephalic record with preservation of all or some of the so-called subcortical components in the rest of the derivations. An interesting dissociation appeared in which some SSEP components were still present in neck-cephalic and spine while absent in scalp-non cephalic leads. Our data further suggested that all components after P13-N13 (recorded with restricted filter bandpass) also recognized two or multiple distinct generator sources. Rostral generators were probably located in the brainstem and/or thalamus, but a significant part of these SSEP components seemed to be generated at the lowest part of the medulla oblongata (dorsal column nuclei) and/or at the level of the upper cervical spine. Visual evoked potentials (VEPs) and the ERG were elicited and recorded simultaneously, using cephalic and non-cephalic references. In all cases in which a non-cephalic reference was used the ERG did not change (either in latency or in morphology) while the VEP channel showed no response. In only two cases (using the VEP derivation with a non-cephalic reference) was it possible to record waves that indicated a spread of the ERG to the occipital area. These results suggested that although contamination of the VEP recordings by the possible spread of the electroretinogram to the occipital area might occur, when using a non-cephalic reference it was easy to confirm the absence of a true cortical visual response in brain-dead patients. It was suggested that the test battery we proposed would permit the assessment of several sensory pathways, in brain-dead patients, thereby considerably increasing diagnostic reliability. Taking into account that these techniques are highly resistant to hypothermia, drug (continued next message) ------------------------------------------------------------------------ @FROM :david@STAT.COM (Continued from last message) intoxication, the use of anesthetics, etc., resort to this battery as confirmatory tests might considerably diminish the time of observation needed to establish a definitive diagnosis of BD. This was of course a fundamental prerequisite to organ transplantation. MEPs and ERG were considered as confirmatory tests in the Cuban Criteria for Brain Death Diagnosis (12). R. Firsching from Germany continued the session, presenting an interesting paper about "Evoked Potentials and Brainstem Reflexes in BD". In Germany registration of brain stem auditory evoked potentials (BAEPs) had been recommended as a confirmatory test of brain death under certain conditions. The author's group investigated 100 patients who exhibited apnoeic coma and cranial nerve arreflexia after primary brain lesions and who finally met all the criteria of brain death. BAEPs, somatosensory (SEP) and visual evoked potentials (VEP) and, in addition, transcranial magnetic (TmgMEP) and electric (TelMEP) motor evoked potentials were registered. In no patient with apnoeic coma and cranial nerve arreflexia could preserve BAEPs, SEP, VEP or TmgMEP or TelMEP. Brainstem reflexes were also abolished with the exception of seven cases with a preserved R1 response of the blink reflex immediately after apnoea had been documented. Registration of evoked potentials as a confirmatory test added safety to the diagnosis of brain death, as they were particularly resistant to drugs. They proved practicable for the declaration of brain death in one third of our patients. Brain stem reflexes required further research. Hilmar Prange, also from Germany, continued the session with some remarks concerning the reliability of several technical investigations for the confirmation of BD. Fifty consecutive patients with suspected brain death were included in his study dedicated to evaluate the reliability of different diagnostic techniques. The techniques employed comprised clinical examination, apnoea testing, EEG, extracranial Doppler ultrasonography (ECD), brainstem acoustic evoked potentials (BAEP) and arterial digital subtraction angiography (DSA). In 39 cases these were no discrepancies in the results of the different techniques used to confirm brain death. With the remaining 11 patients the findings were not exactly concordant or, at least, permitted varying interpretations. For example, in six cases doubts existed as to whether or not the EEG was isoelectric. In four patients BAEP findings were compatible with brain death two to three days before intracranial circulatory arrest was documented. Finally, in two patients with isoelectric EEG and absent BAEP, arterial DSA showed residual cerebral flow. The significance of the mentioned technique for brain death diagnosis was discussed in the light of their conceptual differences implicit in the term brain death. A beautiful lady from Chile, then proved that women were to be respected in neurophysiology. Nelly Chiofallo had worked with Professor Earl Walker during the seventies in an International Commission on Brain Death. She emphasized that when since clinical criteria were only partially realized and there was not total certainty concerning suspected brain death, certain non-invasive electrophysiological tests could provide objective evidence as to whether or not the cerebrum was active. Monitoring EEG and computer-average Evoked Potentials (EP) were among these confirmatory methods. EEG methodology was highly important in relation to both false negatives or false positives findings. (The author's experience with corpses was reported). Dr. Chiofalo presented 132 brain-dead patients studied by EEG, in a three year period, taking into consideration: age-sex distribution, primary diagnosis, consciousness state on admission, time elapsed until respiratory arrest, time elapsed from isoelectric EEG to asystole, etc. She also discussed the utility of topographic brain mapping in a controversial paedriatic case. Minimal EEG activity in few channels were related to artifacts. Mapping-histograms defined the presence of true bioelectrical activity. Flying thousand of miles, A. Erbengy came from Turkey to the Pearl of the Antilles (Cuba). He stressed that although the determination of brain death was fundamentally a clinical diagnosis, conditions that might interfere with diagnostic accuracy required assessment by at least one ancillary test. In his institution (Hacettepe University Medical School) they had found that brain stem auditory evoked potentials (BAEPs) was the most reliable technique. They had also performed radionuclide angiography and brain perfusion studies, whenever they had felt it was necessary. More than 150 brain-dead patients had been studied by BAEPs and 30 by radionuclide angiography and brain perfusion. A highly significant correlation was found among BAEPs and radionuclide study results. None of the patients with absent BAEPs had showed cerebral perfusion. BAEP records, with or without radionuclide studies, had been found to be very reliable adjunct to a clinical diagnosis of brain death. Besides the determination of brain death, radionuclide studies also provided valuable information on the current status of the organs to be used as grafts in organ transplantation (kidneys, liver, heart, etc.) The chairman of this session, Arnold Starr (U. S. A.), had in 1976 reported original data in 1976 about the use of auditory brainstem responses in brain death (18). He now presented a nice lecture entitled "Averaged evoked brain potentials and brain death". The averaging of electrical events in the brain (time-locked to sensory events) revealed a sequence of components reflecting activity at different levels of the pathway from receptor to cerebral cortex. The generators of these components varied, and examples that had been defined included activity in nerve fibers at points of an impedance change or activity in neuronal clusters. In comatose patients, the pattern of potential loss could be used to define the level of brain dysfunction. Brain death had been equated with the loss of central brain or brainstem activity while receptor function could be preserved. Among theoretical problems engendered by these assumptions was the fact that averaging required synchrony of brain activity time-locked to the sensory stimuli. Pathological processes might lead to a loss of this synchrony. Thus even though the brain was viable, averaged evoked potentials might be absent. A pathological process might result in the loss of function of nerve fiber pathways sparing neurons. Averaged evoked potentials would be absent in this scenario, since the neurons would not be receiving input yet the brain would be viable. Compromised receptor function might impair sensory pathway responses in a viable brain. Alternative activation of sensory pathways had to be developed for this situation as it had to be developed with peripheral nerve stimulation for somatosensory evoked potentials. The lunch break proved not only a moment to enjoy cuban food. Three equally attractive lunch panels reported. As a final game for the World Crown in Chess, Christopher Pallis (U. K.) and Earl Walker (U. S. A.) moderated a discussion on the "Brain as a Whole and Whole Brain formulations of death on neurological grounds". Stuart Youngner (U. S. A.) chaired a group of discussion of: The "Higher Brain Formulations of Death". Meanwhile R. Dierkens (Belgium) was accompanied by enthusiastic delegates wanting to discuss "Medical Decisions in Terminal Cases". From Oslo, Marianne Forsman, an interesting nordic lady, presented some remarks about the effect of nimodipine on cerebral flow and cerebrospinal fluid pressure after cardiac arrest. Fifty-one patients were included in a blind randomized study to evaluated whether the Ca-blocker nimodipine could influence cerebral blood flow (CBF) or cerebrospinal fluid pressure (CSFP) during the cerebral hypoperfusion period that followed resuscitation from cardiac arrest and to determined whether changes in CBF correlated with neurologic outcome. CBF (measured 1 to 4 hours after arrest with the use of intravenous 133Xe) was significantly greater with nimodipine than with placebo, There was no clinical evidence of seriously increased CSFP in any patient in either group during the first 48 hours. Mean arterial pressure was significantly lower, and antiarrhythmic drugs were used significantly less frequently in the nimodipine group than in the placebo group. Twelve patients in each group eventually regained consciousness. There was no significant difference in neurologic status between the two groups at any point, and no positive correlation between CBF in the hypoperfusion period and neurologic outcome. From my group, Dr. Orlando Garcia presented the results of a study dealing with heart rate variability (HRV) in coma and brain death. Thirty-three comatose patients were studied serially by HRV and Glasgow Coma Scale (GCS), as were 40 normal subjects to document our normative data. HRV values were considered for different GCS scores. For GCS from 7 to 9, the HRV achieved its maximum values. We considered these in relation to a functional disconnection of the defense hypothalamic area with a normal functioning brainstem, such results apparently not been previously reported in the literature. HRV showed a significant tendency to decrease with low GCS values (3-6). For high GCS scores (10-15), the HRV also showed a significant tendency to decrease. With these results a non-lineal correlation between HRV and GCS was defined. Fourteen brain-dead patients were also studied and were found to present the lowest values for HRV (significantly different from normals). During the atropine test no significant changes in the HRV were found for brain-dead patients. An enthusiastic group of neurologists and neurosurgeons from the Neurological Center of the French Hospital in Buenos Aires, (Argentina) presented three papers dealing with the application of neurophysiological techniques to study brain-dead patients. They described a patient diagnosed as brain dead who had preservation of the spinal (somatosensory) evoked potential at L5-S1. These results might be used to explain the finding of the Lazarus's Sign in brain death. In another paper, they described a series of 30 patients, studied by multi-modality evoked potentials and EEG, finding patterns which confirmed absence of cerebral function. All cases showed a electrocerebral silence, except three patients, who showed preservation of rudimentary but recordable EEG. They discussed the possible mechanisms of EEG preservation in such patients, in relation to the intracranial pathology and to the timing of the EEG study in relation to the clinical evolution, since brain death was established. The colleagues from Argentina were in fact defending the "brain as a whole" (brainstem death) formulation of death. The third paper consisted in the presentation of a patient who developed a cardiac arrest during a study of the brainstem auditory evoked potential. Several changes in evoked responses were noted, that confirmed the diagnosis of brain death. The session devoted to discuss the "Legal Considerations on Brain Death and Related States" was chaired by Professor R. Dierkens, President of the World Association of Medical Law. Dierkens emphasized that the wishes of the patient had to be considered, but in a context in which the medical opinion was also important. The deontological code in Belgium proposed the cessation of treatment when the clinical diagnosis was hopeless. The Catholic Church in this country had also proposed to discontinue treatments progressively in terminal patients, but without abandoning nurse care, pain relief and psychological support. From my group, Dr. Jesus Parets, a young lawyer, continued with "Legal Considerations on Brain Death Diagnosis and the Moment of its Occurrence" . The old Civil Code in Cuba (1942) had stated that "death was diagnosed by physicians confirming an irreversible cessation of cardio-respiratory functions". In 1985 a new Civil Code altered this, starting that "death is diagnosed by physicians in relation to criteria defined by the Ministry of Public Health". This view defended a position in which the relevant criteria were not included in any law. New criteria could thus be included at any time. The Ministry of Public Health had then organized a national commission which every year reviewed and updated the criteria to be applied in our country. A ministerial resolution had validated the use and application of the "Cuban Criteria for Brain Death Diagnosis" (19). DONAR (the Spanish for to donate) is an organization from Santa Fe, Argentina. Its President, Dr. Pedro Zukas, emphasized that "Time is too short for egoism". Dr. Zukas read a paper whose main author was Dr. Cesar Rey Leyes (Argentina). Article 103 of the Argentinean Civil Code emphasized that death made it impossible to have human rights. The diagnosis of death was accepted in relation to medical criteria, but this had to be done independently of any decision concerning organ transplantation. The patient's relatives could give or refuse permission regarding organ donation. The law had to facilitate medical development, and not impede it. A controversial session (Bioethical Considerations on Brain Death and Related States) began in the morning of thursday 24. It was chaired by Daniel Wikler and Stuart Youngner (U. S. A.) An expected lecture was presented by the chairman, Daniel Wikler: "Why Brain-dead Patients are Dead? The President's Commission Explanations After One Decade". Daniel Wikler's presentation was a discussion of the definition of death provided by the President's Commission for the study of Ethical Problems in Medicine and Biomedical and Behavioral Research (11). This commission had been appointed in 1979, by the President of the United States. It had produced eleven reports which had proven influential in American and international bioethics. The President's Commission report addressed three topics: (a) What concept of death should be used? (b) What legal statute should be adopted? (c) How should brain death be diagnosed? However, only (a) was the official product of the Commission. The statute had been written in collaboration with the American Medical Association and the American Bar Association (among others). It gave a legal definition of death as either whole-brain death or cardio-respiratory death. The Commission's report provided (c) as a public service in an Appendix (not endorsed by the Commission itself) its recommendations on diagnosing death. These had been formulated by an expert panel, including Dr. Walker and Dr. Molinari. In its comments on the concept of death (a), the Commission had argued that patients who suffered whole-brain death should be viewed as dead. The primary reason was that the brain (and in particular the brainstem) was the integrator of the body's major organ systems. Without this integration, the Commission reasoned, continued functioning of the patient's major organ systems (in an ICU) did not constitute organismic life. The Commission rejected a "cortical-death" definition, pointing out that such a definition of death would seem to endorse the burial of a patient with a spontaneously beating heart. The Commission's findings had resulted in a change in the definition of death in nearly every one of the states in the U. S. A. (where defining death is a matter of state, rather than federal, law). Philosophers, however, had questioned the logic of the Commission's central argument, pointing out that the major organ systems in a well-maintained brain-dead patient, interacted so as to sustain the main non-cognitive bodily functions. Dr. Stuart Youngner (Associate Professor of Medicine, Psychiatry and Biomedical Ethics at the Case Western Reserve University School of Medicine and Director of the Clinical Ethics Program of the University Hospitals of Cleveland) presented a paper on "Brain Death and Organ Transplantation: Confusion and Its Consequences" (20). He argued that despite the rapid and widespread embrace of so-called "brain death" in the United States, confusion about its meaning and implications remained a problem. He gave several examples of evidence of this confusion. First, the criterion of brain death, i.e the irreversible loss of all brain function, was accepted for practical reasons (without a wide agreement on exactly why patients who had lost all brain function were dead). The practical reasons were: (1) in the hands of a competent neurologist, neurosurgeon, or critical care physician, brain death was a relatively easy diagnosis to make; and (2) that once the diagnosis of brain death had been made the prognosis was certain that the patient would never regain consciousness and would develop asystole within a short time, despite continued aggressive intervention. The diagnostic certainty and uniformly dismal cardiac prognosis for brain-dead patients facilitated the acceptance of policies aimed at treatment withdrawal and organ retrieval. A study by Youngner and his colleagues (20) at Case Western Reserve University had, however, indicated that physicians and nurses working in critical care and operating room settings accepted brain death for different reasons. Some thought brain-dead patients were dead because they would never wake up again. Others accepted them as dead because they had lost the integrating functions of the brainstem. Still others indicated that they did not really believe the patients were dead, saying that the patients were "going to die very soon despite aggressive treatment" or that their "quality of life was unacceptable." Further evidence of confusion was the stubborn persistence of the term "brain death" itself. Health professionals consistently referred to patients who had lost all brain function as brain-dead (rather than, simply dead). It is also common to hear them say that the brain-dead patient "died" after life support had been removed. Of course you can not die if you are already dead. The persistence of term brain death may well reflect an inevitable conflict between reason (which told us that brain-dead patients were dead) and emotions. The latter were stimulated by the many signs of "life" still shown in brain-dead patients. These were of particular concern to nurses who took care of brain-dead patients. Intensive Care Unit nurses reported feelings of discomfort at calling patients "dead" who require aggressive treatment (including (continued next message) ------------------------------------------------------------------------ @FROM :david@STAT.COM (Continued from last message) resuscitative efforts if the "dead" patient develop a cardiac arrests) at a time when clearly living and conscious patients, in the same unit, fell into the "do not resuscitate" category. In the operating theater, nurses sometimes felt that the patient's spirit was in the room during organ retrieval surgery, and only departed when the ventilator was turned off and the patient came to complete rest. These examples of confusion were inevitable when we were willing to call patients dead when so much life persisted. This confusion pointed not only to the need for more ongoing education about brain death, but also for wide debate and consensus among various elements of society (including not only doctors, but the legal and religious communities, and especially the lay public) before policies are implemented and enforced. To do otherwise was to foment distrust and suspicion of medical science, perhaps undermining the worthwhile goal of saving more lives by getting more persons to donate their organs. Dr. E. Bochiardo from DONAR (Argentina) presented a paper "Brain Death", in which he emphasized that until some time ago the determination of death was relatively easy: confirming the irreversible absence of cardio-respiratory function. In the sixties, the development of reanimation and other intensive care techniques, forced physicians to confront the concept of brain death. A man had to be considered dead when his brain functions disappeared. He considered that the decision (made by patient's relatives) to donate organs was a transcendental and admirable token. The results of an interesting survey were then presented by Dr. Eduardo Fermin, a delegate of the Cuban group. The subject of the survey was related to the decisions and feelings of the physician, who had to decide what to do in a brain-dead patient, when transplantation was not envisaged. The survey described to the attitudes of 50 specialists in intensive care medicine. This survey was anonymous, assessing the concepts of life and death, euthanasia, as well as the methods used in the process of diagnosing brain death. Many interesting results had arisen: for example, the confusion about methods and criteria for diagnosing death, concerns about the legal protection of physicians, doubts about when to turn-off the respirator, mistakes in the concepts of BD and euthanasia, etc. Many physicians had expressed religious opinions in this context. Two cuban specialists in psychiatry (Drs. Jose A. Hernandez and Carlos M. Notario) ended this session presenting a paper entitled: "Attention to Near-Death-Patients". They appreciated the classic study of Dr. Klubler-Ross and particularly her description of the psychological stages in dying persons. They paid attention to the medical custom which sought to prolong, in all possible ways, the life of hopelessly ill patients, while accepting that medical procedures should be directed to relieve the pain of the dying and allowing a decorous death. They stated that their purpose was to stimulate a discussion about this subject in our country and to exchange opinions with foreign experts, but always keeping their patients in the forefront of their minds. Three interesting lunch panels joined delegates with providing food for thought. "Near-death Experiences" was chaired by the Reverend Douglas Lynn (Canada), "Organ Marketing" by Dr. Raul Herrera (Cuba) and "Transplant Alternatives" by Dr. Noel Gonzalez (Cuba). "Brain Death in Children" is always a controversial subject. This session was chaired by Dr. Kimio Sainio from Finland. He opened the session with a study of the patients with suspected brain death seen in the Children's University Hospital of Helsinki, during a ten year period (1983-1992). The study correlated clinical, neuroradiological and EEG data. A total of 36 patients were studied, ranging in age from 0 days to 11 years (mean = 1.9). Brain death was diagnosed in 21 patients. The diagnosis was confirmed in three patients by cerebral angiography and in four patients by colour flow Doppler ultrasound examinations. The EEG was inactive in 19 patients. Two patients showed minimal EEG activity two to five days before brain death was confirmed. The diagnosis of BD was not confirmed in 15 patients. Five of these cases had either flat or burst-suppression EEGs. Four of them died and one survived with major neurological sequelae. The inactivity of the EEG was due to barbiturate medication in two patients; both survived with major neurological sequelae. Both EEG and Doppler examinations were compatible with brain death, while clinically some brainstem function persisted in these two cases; both developed asystole within 24 hours. 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